RNA quality control nonsense-mediated decay is involved in viral restriction in both plants and animals.However,it is not known whether two other RNA quality control pathways,nonstop decay and no-go decay,are capable ...RNA quality control nonsense-mediated decay is involved in viral restriction in both plants and animals.However,it is not known whether two other RNA quality control pathways,nonstop decay and no-go decay,are capable of restricting viruses in plants.Here,we show that the evolutionarily conserved Pelota–Hbs1 complex negatively regulates infection of plant viruses in the family Potyviridae(termed potyvirids),the largest group of plant RNA viruses that accounts for more than half of the viral crop damage worldwide.Pelota enables the recognition of the functional G1-2A6-7 motif in the P3 cistron,which is conserved in almost all potyvirids.This allows Pelota to target the virus and act as a viral restriction factor.Furthermore,Pelota interacts with the SUMO E2-conjugating enzyme SCE1 and is SUMOylated in planta.Blocking Pelota SUMOylation disrupts the ability to recruit Hbs1 and inhibits viral RNA degradation.These findings reveal the functional importance of Pelota SUMOylation during the infection of potyvirids in plants.展开更多
A complex network of cellular receptors,RNA targeting pathways,and small-molecule signaling provides robust plant immunity and tolerance to viruses.To maximize their fitness,viruses must evolve control mechanisms to b...A complex network of cellular receptors,RNA targeting pathways,and small-molecule signaling provides robust plant immunity and tolerance to viruses.To maximize their fitness,viruses must evolve control mechanisms to balance host immune evasion and plant-damaging effects.The genus Potyvirus comprises plant viruses characterized by RNA genomes that encode large polyproteins led by the P1 protease.A P1 autoinhibitory domain controls polyprotein processing,the release of a downstream functional RNAsilencing suppressor,and viral replication.Here,we show that P1Pro,a plum pox virus clone that lacks the P1 autoinhibitory domain,triggers complex reprogramming of the host transcriptome and high levels of abscisic acid(ABA)accumulation.A meta-analysis highlighted ABA connections with host pathways known to control RNA stability,turnover,maturation,and translation.Transcriptomic changes triggered by P1Pro infection or ABA showed similarities in host RNA abundance and diversity.Genetic and hormone treatment assays showed that ABA promotes plant resistance to potyviral infection.Finally,quantitative mathematical modeling of viral replication in the presence of defense pathways supported self-control of polyprotein processing kinetics as a viral mechanism that attenuates the magnitude of the host antiviral response.Overall,our findings indicate that ABA is an active player in plant antiviral immunity,which is nonetheless evaded by a self-controlled RNA virus.展开更多
基金funded by the National Key Research and Development Program of China(2021YFD1400400)National Natural Science Foundation of China(31972244)to F.L.
文摘RNA quality control nonsense-mediated decay is involved in viral restriction in both plants and animals.However,it is not known whether two other RNA quality control pathways,nonstop decay and no-go decay,are capable of restricting viruses in plants.Here,we show that the evolutionarily conserved Pelota–Hbs1 complex negatively regulates infection of plant viruses in the family Potyviridae(termed potyvirids),the largest group of plant RNA viruses that accounts for more than half of the viral crop damage worldwide.Pelota enables the recognition of the functional G1-2A6-7 motif in the P3 cistron,which is conserved in almost all potyvirids.This allows Pelota to target the virus and act as a viral restriction factor.Furthermore,Pelota interacts with the SUMO E2-conjugating enzyme SCE1 and is SUMOylated in planta.Blocking Pelota SUMOylation disrupts the ability to recruit Hbs1 and inhibits viral RNA degradation.These findings reveal the functional importance of Pelota SUMOylation during the infection of potyvirids in plants.
基金supported by funds to J.A.G.from the Ministerio de Ciencia e Innovaciòn(Spain),grants BIO2016-80572-R and PID2019-109380RBI00/AEI/10.13039/501100011033(AEI-FEDER)funded by grant K124705 from the National Research Development and Innovation Office(Hungary)+2 种基金S.M.-B.by grant 2017 SGR 980 from the Generalitat de Catalunya(Spain)supported by NIH grant HG006620the recipient of a post-doctoral fellowship from Academia Sinica(Taiwan).
文摘A complex network of cellular receptors,RNA targeting pathways,and small-molecule signaling provides robust plant immunity and tolerance to viruses.To maximize their fitness,viruses must evolve control mechanisms to balance host immune evasion and plant-damaging effects.The genus Potyvirus comprises plant viruses characterized by RNA genomes that encode large polyproteins led by the P1 protease.A P1 autoinhibitory domain controls polyprotein processing,the release of a downstream functional RNAsilencing suppressor,and viral replication.Here,we show that P1Pro,a plum pox virus clone that lacks the P1 autoinhibitory domain,triggers complex reprogramming of the host transcriptome and high levels of abscisic acid(ABA)accumulation.A meta-analysis highlighted ABA connections with host pathways known to control RNA stability,turnover,maturation,and translation.Transcriptomic changes triggered by P1Pro infection or ABA showed similarities in host RNA abundance and diversity.Genetic and hormone treatment assays showed that ABA promotes plant resistance to potyviral infection.Finally,quantitative mathematical modeling of viral replication in the presence of defense pathways supported self-control of polyprotein processing kinetics as a viral mechanism that attenuates the magnitude of the host antiviral response.Overall,our findings indicate that ABA is an active player in plant antiviral immunity,which is nonetheless evaded by a self-controlled RNA virus.